Journal ArticleDOI
Normalization of Plasma Lipid Peroxides, Monocyte Adhesion, and Tumor Necrosis Factor-α Production in NIDDM Patients After Gliclazide Treatment
TLDR
Gliclazide administration to NIDDM patients inhibits the increased adhesiveness of diabetic monocytes to endothelial cells and reduces the production of TNF-α by these cells, suggesting that treatment of N IDDM subjects with gliclazer may be beneficial in the prevention of atherosclerosis associated with NID DM.Abstract:
OBJECTIVE To evaluate the effect of gliclazide administration to NIDDM patients on 1) monocyte adhesion to cultured endothelial cells, 2) plasma cytokine and lipid peroxide levels, and 3) monocyte cytokine production. RESEARCH DESIGN AND METHODS Poorly controlled glyburide-treated diabetic patients ( n = 8) and healthy control subjects ( n = 8) were recruited. At the beginning of the study, glyburide was replaced by an equivalent hypoglycemic dose of gliclazide. Serum and monocytes were isolated from blood obtained from control and diabetic subjects before and after 3 months of treatment with gliclazide. RESULTS Plasma lipid peroxide levels and monocyte adhesion to endothelial cells are enhanced in NIDDM patients, and gliclazide administration totally reverses these abnormalities. Before gliclazide treatment, serum levels of cytokines did not differ in the control and the diabetic groups, with the exception of an enhancement of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL)-6 in NIDDM subjects. Basal and lipopolysaccharide (LPS)-stimulated monocyte production of interleukin-1β, IL-6, and IL-8 did not differ between the two groups. Furthermore, basal monocyte production of TNF-α was similar in the control and the diabetic groups, whereas a marked increase in the LPS-stimulated monocyte production of TNF-α was observed in the NIDDM group. Gliclazide treatment lowered LPS-stimulated TNF-α production by diabetic monocytes to levels similar to those observed in control subjects. CONCLUSIONS Gliclazide administration to NIDDM patients inhibits the increased adhesiveness of diabetic monocytes to endothelial cells and reduces the production of TNF-α by these cells. These results suggest that treatment of NIDDM subjects with gliclazide may be beneficial in the prevention of atherosclerosis associated with NIDDM.read more
Citations
More filters
Journal ArticleDOI
Obesity, inflammation, and insulin resistance.
TL;DR: The rapidly expanding body of animal and clinical data that support potential roles for inflammation in the pathogenesis of insulin resistance and type 2 diabetes mellitus are reviewed.
Journal ArticleDOI
Adipocytokines and Insulin Resistance
TL;DR: This work reviews potential insulin sensitizers such as leptin and adiponectin or insulin antagonists such as resistin, TNF, and IL-6 and focuses on certain adipocytokines and how they influence insulin sensitivity.
Journal ArticleDOI
Critical review of acylation-stimulating protein physiology in humans and rodents
TL;DR: A comprehensive overview of the recent literature on acylation-stimulating protein is provided, with particular emphasis on those studies carried out in rodents and humans.
Journal ArticleDOI
Monocytes from type 2 diabetic patients have a pro-inflammatory profile. 1,25-Dihydroxyvitamin D(3) works as anti-inflammatory.
Annapaula Giulietti,Evelyne van Etten,Lutgart Overbergh,Katinka Stoffels,Roger Bouillon,Chantal Mathieu +5 more
TL;DR: It is concluded that monocytes from type 2 diabetic patients have a pro-inflammatory profile and 1,25-dihydroxyvitamin D(3), the active form of Vitamin D, as an anti-inflammatory agent was able to modulate inflammation in these monocytes.
Journal ArticleDOI
Molecular Mechanisms of Tumor Necrosis Factor α Gene Expression in Monocytic Cells via Hyperglycemia-induced Oxidant Stress-dependent and -independent Pathways
TL;DR: It is demonstrated that chronic high glucose causes a dramatic increase in the release of the inflammatory cytokine tumor necrosis factor α (TNFα), at least in part through enhanced TNFα mRNA transcription, mediated by ROS via activation of transcription factors nuclear factor κB (NF-κB) and activating protein-1 (AP-1).
References
More filters
Journal ArticleDOI
Beyond cholesterol, modifications of low-density lipoprotein that increase its atherogenicity
Journal ArticleDOI
Determination of malonaldehyde precursor in tissues by thiobarbituric acid test
Mitsuru Uchiyama,Midori Mihara +1 more
TL;DR: It was concluded that the deproteinization of homogenate prior to coloration is not needed, but double wavelength measurement is necessary to avoid interference and the reaction should be performed with phosphoric acid at a definite pH near 2.0.
Journal ArticleDOI
Minimally modified low density lipoprotein stimulates monocyte endothelial interactions
Judith A. Berliner,Mary C. Territo,Alex Sevanian,S Ramin,J A Kim,B Bamshad,M Esterson,A M Fogelman +7 more
TL;DR: It is concluded that exposure of EC to sublethal levels of MM-LDL enhances monocyte endothelial interactions and induces resistance to the toxic effects of MM -LDL.
Journal ArticleDOI
Reduced tyrosine kinase activity of the insulin receptor in obesity-diabetes. Central role of tumor necrosis factor-alpha.
TL;DR: It is demonstrated that TNF-alpha participates in obesity-related systemic insulin resistance by inhibiting the IR tyrosine kinase in the two tissues mainly responsible for insulin-stimulated glucose uptake: muscle and fat.